Publications by authors named "E Cormet-Boyaka"
Secondhand vape exposure regulation of CFTR and immune function in cystic fibrosis.
Am J Physiol Lung Cell Mol Physiol
January 2025
Secondhand smoke exposure (SHSe) is a public health threat for people with cystic fibrosis (CF) and other lung diseases. Primary smoking reduces CFTR channel function, the causative defect in CF. We reported that SHSe worsens respiratory and nutritional outcomes in CF by disrupting immune responses and metabolic signaling.
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- Researchers developed enhanced single-stranded DNA (esDNA) templates with chemical modifications that significantly improve the efficiency of genome editing when used with Cas9, achieving 2-3 times higher knock-in rates compared to standard ssDNA.
- In specific cell types, such as airway basal stem cells and CD34+ hematopoietic cells, esDNA facilitated correction of target genes (CFTR, HBB, CCR5) in over 50% of cases, indicating strong potential for therapeutic applications.
- However, esDNA wasn't effective in induced pluripotent stem cells due to the lack of the nuclease TREX1, suggesting further research is needed for scalable production of modified ssDNA for gene insertion.
Article Synopsis
- * Previous gene-editing techniques using CRISPR-Cas9 had low efficiency (<10%) in enhancing CFTR function, necessitating further advancements in gene insertion methods for better therapy outcomes.
- * Using small molecules AZD7648 and ART558 improved cDNA insertion in airway stem cells, though ART558 introduced toxicity; AZD7648 alone significantly boosted gene insertion without increasing off-target effects, warranting further research for safety and efficacy.
Cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator () gene. Although many people with CF (pwCF) are treated using CFTR modulators, some are non-responsive due to their genotype or other uncharacterized reasons. Autologous airway stem cell therapies, in which the cDNA has been replaced, may enable a durable therapy for all pwCF.
View Article and Find Full Text PDFObesity has been associated with dysbiosis, but innate mechanisms linking intestinal epithelial cell subsets and obesity remain poorly understood. Using mice lacking Paneth cells (Sox9 mice), small intestinal epithelial cells specialized in the production of antimicrobial products and cytokines, we show that dysbiosis alone does not induce obesity or metabolic disorders. Loss of Paneth cells reduced ILC3 and increased ILC2 numbers in the intestinal lamina propria.
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